Overview Show Antidiuretic hormone (ADH) is produced by an area of the brain called the hypothalamus. This hormone is stored in and released by the pituitary gland. ADH controls how your body releases and conserves water. When ADH (also called vasopressin) is produced in excess, the condition is called syndrome of inappropriate antidiuretic hormone (SIADH). This overproduction can occur in places other than the hypothalamus. SIADH makes it harder for your body to release water. Additionally, SIDAH causes levels of electrolytes, like sodium, to fall as a result of water retention. A low sodium level or hyponatremia is a major complication of SIADH and is responsible for many of the symptoms of SIADH. Early symptoms may be mild and include cramping, nausea, and vomiting. In severe cases, SIADH can cause confusion, seizures, and coma. Treatment usually begins with limiting fluid intake to prevent further buildup. Additional treatment will depend on the cause. Another name for the syndrome is “ectopic ADH secretion.” A variety of conditions can trigger abnormal ADH production, including:
SIADH makes it difficult for your body to get rid of excess water. This causes a buildup of fluids as well as abnormally low sodium levels. Symptoms may be mild and vague at first, but tend to build. Severe cases may involve these symptoms:
Your doctor will ask for your complete medical history and current symptoms. Your doctor should know whether you are taking any over-the-counter or prescription medications or supplements. Diagnosis usually begins with a physical exam. Often, a urine sample is also required. Blood tests, specifically one called an ADH test, can measure circulating ADH levels in the blood, but it’s very difficult to obtain an accurate level. According to the University of Rochester Medical Center, normal values for ADH range from 0-5 picograms per milliliter. Higher levels could be the result of SIADH. Most cases of SIADH are accurately diagnosed using serum and urine sodium and osmolality values as well as clinical presentation. Following diagnosis of SIADH, the next step will be to identify the condition that caused it to occur. The first line of treatment is to limit fluid intake to avoid further buildup. Medications may include those that can reduce fluid retention, such as furosemide (Lasix), and those that can inhibit ADH, like demeclocycline. Your prognosis will depend on the cause of SIADH. Any underlying medical conditions must be treated. 1. Piek J. Medical complications in severe head injury. New Horiz. 1995; 3:534–538. PMID: 7496764. 2. Arango MF, Andrews PJ. Systemic complications of neurologic diseases. Curr Opin Crit Care. 2001; 7:61–67. PMID: 11373512. 3. Tisdall M, Crocker M, Watkiss J, Smith M. Disturbances of sodium in critically ill adult neurologic patients: a clinical review. J Neurosurg Anesthesiol. 2006; 18:57–63. PMID: 16369141. 4. Davenport A. The brain and the kidney--organ cross
talk and interactions. Blood Purif. 2008; 26:526–536. PMID: 18987466. 5. Swaab DF, Nijveldt F, Pool CW. Distribution of oxytocin and vasopressin in the rat supraoptic and paraventricular nucleus. J Endocrinol. 1975; 67:461–462. PMID: 1206330. 6. Sachs H, Poryanova R, Haller EW, Share L. Cellular processes concerned with vasopressin biosynthesis, storage and release. Neurosecretion. 1967. 1st ed. Berlin: Springer-Verlag;p. 146–154. 7. Robertson GL. Antidiuretic hormone. Normal and disordered function. Endocrinol Metab Clin North Am. 2001; 30:671–694. PMID: 11571936. 8. Robertson GL, Aycinena P, Zerbe RL. Neurogenic disorders of osmoregulation. Am J Med. 1982; 72:339–353. PMID:
7036730. 9. Landry DW, Oliver JA. The pathogenesis of vasodilatory shock. N Engl J Med. 2001; 345:588–595. PMID: 11529214. 10. McKinley MJ, Mathai ML, McAllen RM, et al. Vasopressin secretion: osmotic and hormonal regulation by the lamina terminalis. J Neuroendocrinol. 2004; 16:340–347. PMID: 15089972. 11. Baumann G, Dingman JF. Distribution, blood transport, and degradation of antidiuretic hormone in man. J Clin Invest. 1976; 57:1109–1116. PMID: 1262458. 12. Verbalis JG. Vasopressin V2 receptor antagonists. J Mol Endocrinol. 2002; 29:1–9. PMID: 12200224. 13.
Nielsen S. Renal aquaporins: an overview. BJU Int. 2002; 90(Suppl 3):1–6. PMID: 12445090. 14. Flear CT, Gill GV, Burn J. Hyponatraemia: mechanisms and management. Lancet. 1981; 2:26–31. PMID:
6113402. 15. Waikar SS, Mount DB, Curhan GC. Mortality after hospitalization with mild, moderate, and severe hyponatremia. Am J Med. 2009; 122:857–865. PMID: 19699382. 16. Reeder RF, Harbaugh RE. Administration of intravenous urea and normal saline for the treatment of hyponatremia in neurosurgical patients. J Neurosurg. 1989; 70:201–206. PMID: 2913218. 17. Hasan D, Wijdicks EF, Vermeulen M. Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Ann Neurol. 1990; 27:106–108. PMID: 2301918. 18. Karandanis D, Shulman JA. Recent survey of infectious meningitis in adults: review of laboratory findings in bacterial, tuberculous, and aseptic meningitis. South Med J. 1976; 69:449–457. PMID: 1265506. 19. Sane T, Rantakari K, Poranen A, Tahtela R,
Valimaki M, Pelkonen R. Hyponatremia after transsphenoidal surgery for pituitary tumors. J Clin Endocrinol Metab. 1994; 79:1395–1398. PMID: 7962334. 20. Olson BR, Gumowski J, Rubino D, Oldfield EH. Pathophysiology of hyponatremia after transsphenoidal pituitary
surgery. J Neurosurg. 1997; 87:499–507. PMID: 9322839. 21. Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med. 2000; 342:1581–1589. PMID: 10824078. 22. Boulard G, Marguinaud E, Sesay M. Osmotic cerebral oedema: the role of plasma osmolarity and blood brain barrier. Ann Fr Anesth Reanim. 2003; 22:215–219. PMID: 12747989. 23. Wijdicks EF, Vermeulen M, Hijdra A, van Gijn J. Hyponatremia and
cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? Ann Neurol. 1985; 17:137–140. PMID: 3977297. 24. Rabinstein AA, Wijdicks EF. Hyponatremia in critically ill neurological patients. Neurologist. 2003; 9:290–300.
PMID: 14629783. 25. Robertson GL. Regulation of arginine vasopressin in the syndrome of inappropriate antidiuresis. Am J Med. 2006; 119:S36–S42. PMID: 16843083. 26. Smith D, Moore K, Tormey W, Baylis PH, Thompson CJ. Downward resetting of the osmotic threshold for thirst in patients with SIADH. Am J Physiol Endocrinol Metab. 2004; 287:E1019–E1023. PMID: 15213060. 27. Palmer BF. Hyponatremia in patients with central nervous system disease: SIADH versus CSW. Trends Endocrinol Metab. 2003; 14:182–187. PMID: 12714279. 28. Maesaka JK, Imbriano LJ, Ali NM, Ilamathi E. Is it cerebral or renal salt wasting? Kidney Int. 2009; 76:934–938. PMID: 19641485. 29. Ellison DH, Berl T. Clinical practice. The syndrome of inappropriate antidiuresis. N Engl J Med. 2007; 356:2064–2072. PMID: 17507705. 30. Bhardwaj A. Neurological impact of vasopressin dysregulation and hyponatremia. Ann Neurol. 2006; 59:229–236. PMID:
16437573. 31. Casulari LA, Costa KN, Albuquerque RC, Naves LA, Suzuki K, Domingues L. Differential diagnosis and treatment of hyponatremia following pituitary surgery. J Neurosurg Sci. 2004; 48:11–18. PMID:
15257260. 32. Palmer BF, Gates JR, Lader M. Causes and management of hyponatremia. Ann Pharmacother. 2003; 37:1694–1702. PMID: 14565794. 33. Laureno R, Karp BI. Myelinolysis after
correction of hyponatremia. Ann Intern Med. 1997; 126:57–62. PMID: 8992924. 34. Rabinstein AA. Vasopressin antagonism: potential impact on neurologic disease. Clin Neuropharmacol. 2006; 29:87–93. PMID:
16614541. 35. Sherlock M, O'Sullivan E, Agha A, et al. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf). 2006; 64:250–254. PMID: 16487432. 36. Palmer BF. Hyponatraemia in a neurosurgical patient: syndrome of inappropriate antidiuretic hormone secretion versus cerebral salt wasting. Nephrol Dial Transplant. 2000; 15:262–268. PMID: 10648680. 37. Berendes E, Walter M, Cullen P, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet. 1997; 349:245–249. PMID: 9014912. 38. Schweda F, Friis U, Wagner C, Skott O, Kurtz A. Renin release. Physiology (Bethesda). 2007; 22:310–319. PMID: 17928544. 39. Marin-Grez M, Fleming JT, Steinhausen M. Atrial natriuretic peptide causes pre-glomerular vasodilatation and postglomerular vasoconstriction in rat kidney. Nature. 1986; 324:473–476. PMID: 2946962. 40. Levin ER, Gardner DG, Samson WK. Natriuretic peptides. N Engl J Med. 1998; 339:321–328. PMID: 9682046. 41. Maesaka JK, Gupta S, Fishbane S. Cerebral salt-wasting syndrome: does it exist? Nephron. 1999; 82:100–109. PMID: 10364700. 42. Bitew S, Imbriano L, Miyawaki N, Fishbane S, Maesaka JK. More on renal salt wasting without cerebral disease: response to saline
infusion. Clin J Am Soc Nephrol. 2009; 4:309–315. PMID: 19201917. 43. Hasan D, Lindsay KW, Wijdicks EF, et al. Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage. Stroke. 1989; 20:1156–1161. PMID:
2672426. What electrolyte disorder is associated with SIADH?Hyponatraemia is the commonest electrolyte abnormality found in hospital inpatients, and is associated with a greatly increased morbidity and mortality. The syndrome of inappropriate antidiuretic hormone (SIADH) is the most frequent cause of hyponatraemia in hospital inpatients.
What is associated with the syndrome of inappropriate secretion of ADH?SIADH happens when your body makes excess amounts of antidiuretic hormone (ADH). SIADH causes your body to retain too much water and commonly leads to hyponatremia, which is low levels of sodium in your blood. It's treatable.
What causes syndrome of inappropriate antidiuretic hormone?SIADH tends to occur in people with heart failure or people with a diseased hypothalamus (the part of the brain that works directly with the pituitary gland to produce hormones). In other cases, a certain cancer (elsewhere in the body) may produce the antidiuretic hormone, especially certain lung cancers.
Does ADH cause Hypo or hypernatremia?Hyponatremia is mediated initially by ADH-induced water retention that results in volume expansion which activities secondary natriuretic mechanisms causing sodium and water loss and restoration of euvolemia.
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